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Formononetin Inhibits Non-Small Cell Lung Cancer Proliferation via Regulation of mir-27a-3p through p53 Pathway

Chunya Hu, Yu He*
Institute of Chinese Medicine Chemistry, Zhejiang University of Traditional Chinese Medicine, Hangzhou, 310053, China
* Corresponding Author: Yu He. Email:

Oncologie 2021, 23(2), 241-250. 10.32604/Oncologie.2021.015828

Received 17 January 2021; Accepted 25 March 2021; Issue published 22 June 2021


Objective: The aim of the present study was to investigate the anti-tumor effects of formononetin on human nonsmall cell lung cancer (NSCLC) and its potential molecular mechanism. Methods: A549 cells were treated with different concentrations of formononetin, then detected the cell proliferation, apoptosis and the expression of HIPK2 respectively by MTT assay, flow cytometry analysis and RT-qPCR. Then the interaction between miR- 27a-3p and its target gene HIPK2 was verified through luciferase reporter assay. The expression of miR-27a- 3p, HIPK2, and p53 was detected after being treated with different formononetin concentrations by RT-qPCR and western blot. Results: The results showed that formononetin significantly inhibited the proliferation and induced the apoptosis of A549 cells in a time- and dose-dependent manner. miR-27a-3p targeted HIPK2 3’UTR and inhibited the expression of HIPK2. Also, formononetin-treated A549 cells were remarked with a significant decline in the expression of miR-27a-3p, accompanied with growth of HIPK2, and subsequently a reduction of p53. Conclusions: The study indicates that miR-27a-3p might pose regulated effects on the HIPK2/p53 pathway, resulting in formononetin’s anti-carcinogenic effects on NSCLC in vitro.


Non-small cell lung cancer (NSCLC); formononetin; miRNA; anti-cancer; p53 pathway

Cite This Article

Hu, C., He, Y. (2021). Formononetin Inhibits Non-Small Cell Lung Cancer Proliferation via Regulation of mir-27a-3p through p53 Pathway. Oncologie, 23(2), 241–250.

This work is licensed under a Creative Commons Attribution 4.0 International License , which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
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